Hyperbilirubinemia develops when bilirubin production exceeds the newborn’s ability to conjugate and eliminate it. The mechanism may be physiologic, feeding-related, hemolytic, obstructive, infectious, metabolic, or related to bruising and blood breakdown. Physiologic jaundice usually appears after the first 24 hours of life, peaks around days 3 to 5 in term newborns, and resolves as feeding improves and liver conjugation matures. This is expected newborn adaptation, but it still requires screening and follow-up. Suboptimal intake hyperbilirubinemia occurs when milk transfer is inadequate. The issue is not breastfeeding itself; the problem is insufficient intake. Poor intake leads to dehydration risk, fewer stools, delayed bilirubin elimination, and increased enterohepatic circulation. The AAP uses the term “suboptimal intake hyperbilirubinemia” rather than “breastfeeding jaundice” because the cause is inadequate intake, not breastfeeding as a practice. Breast milk jaundice is different. It occurs in a thriving breastfed infant with good intake, appropriate weight gain, and persistent unconjugated hyperbilirubinemia. It may last for weeks and is usually benign, but prolonged jaundice still needs evaluation to rule out direct hyperbilirubinemia, cholestasis, hypothyroidism, galactosemia, hemolysis, and other pathology. The...